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Inflamm Res. 2012 Mar;61(3):197-205. doi: 10.1007/s00011-011-0401-y. Epub 2011 Nov 25.

Severe neutrophil-mediated lung inflammation in myeloperoxidase-deficient mice exposed to zymosan.

Author information

1
Graduate School of Nanobioscience, Yokohama City University, Seto 22-2, Kanazawa, Yokohama 236-0027, Japan.

Abstract

OBJECTIVE AND DESIGN:

This study examines the role of myeloperoxidase (MPO), a major constituent of neutrophils that generates hypochlorous acid, in neutrophil recruitment into the zymosan-exposed lung of mice.

METHODS:

Mice were inoculated intranasally with zymosan. The accumulation of neutrophils and other inflammatory cells within the lung was analyzed by flow cytometry. Macrophage inflammatory protein 2 (MIP-2) expression in the lung was quantified, and the contribution of this chemokine to neutrophil accumulation was examined by intranasal administration of MIP-2 antibody. The cellular sources of MIP-2 were identified, and the production of this chemokine from macrophages and neutrophils was quantified in vitro.

RESULTS:

Zymosan exposure led to greater neutrophil infiltration into the lungs of MPO(-/-) mice relative to wild-type mice. This was associated with higher MIP-2 levels in the mutant mice. Neutralization of MIP-2 in vivo significantly reduced neutrophil infiltration. Neutrophils from MPO(-/-) mice produced more MIP-2, and the production was reduced when MPO was added exogenously.

CONCLUSIONS:

MPO deficiency results in severe lung inflammation in mice exposed to zymosan. Relatively high MIP-2 levels likely contribute to the strong inflammatory response in these animals.

PMID:
22116298
DOI:
10.1007/s00011-011-0401-y
[Indexed for MEDLINE]

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